Abstract
Anaphylactic shock can be defined as an acute syndrome, and it is the most severe clinical manifestation of allergic diseases. Anaphylactoid reactions are similar to anaphylactic events but differ in the pathophysiological mechanism. Nitric oxide (NO) inhibitors during anaphylaxis suggest that NO might decrease the signs and symptoms of anaphylaxis but exacerbate associated vasodilation. Therefore, blocking the effects of NO on vascular smooth muscle by inhibiting the guanylate cyclase (GC) would be a reasonable strategy. This study aimed to investigate the effects of NO/cGMP pathway inhibitors methylene blue (MB), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), and indigo carmine (IC) in shock induced by compound 48/80 (C48/80) in rats. The effect was assessed by invasive blood pressure measurement. Shock was initiated by C48/80 intravenous bolus injection 5 min before (prophylactic) or after (treatment) the administration of the inhibitors MB (3 mg/kg), L-NAME (1 mg/kg), and IC (3 mg/kg). Of the groups that received drugs as prophylaxis for shock, only the IC group did not present the final systolic blood pressure (SBP) better than the C48/80 group. Regarding shock treatment with the drugs tested, all groups had the final SBP similar to the C48/80group. Altogether, our results suggested that inhibition of GC and NO synthase in NO production pathway was not sufficient to revert hypotension or significantly improve survival.
Highlights
Anaphylactic shock can currently be defined as an acute syndrome, the most severe clinical manifestation of allergic diseases
This study aimed to investigate the effects of Nitric oxide (NO)/ cyclic guanosine monophosphate (cGMP) pathway inhibitors [methylene blue (MB), No-nitroL-arginine methyl ester hydrochloride (L-NAME), and indigo carmine (IC)] in the treatment of induced shock by compound 48/80 (C48/80) in rats
C48/80 was efficient in shock induction because the rats presented hypotension, characteristic clinical signs such as cyanotic ears, paws, and tongue, and respiratory distress
Summary
Anaphylactic shock can currently be defined as an acute syndrome, the most severe clinical manifestation of allergic diseases. Fatal, it is a type I hypersensitivity reaction against specific antigens, leading to the formation of antibodies [1]. The reaction requires sensitization to a particular substance which, on contact, produces immunoglobulin E (IgE) against the immunogen. When a new exposure occurs, the immune system responds immediately to mast cell degranulation [2,3,4]. Anaphylactoid reactions are like anaphylactic manifestations but differ in the pathophysiological mechanism. The pathogenesis of anaphylaxis typically involves IgEdependent events, and the anaphylactoid responses include IgE-independent results that otherwise are clinically indistinguishable [1,5]
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